HIV mutation literature information.


  The Y181C substitution in 3'-azido-3'-deoxythymidine-resistant human immunodeficiency virus, type 1, reverse transcriptase suppresses the ATP-mediated repair of the 3'-azido-3'-deoxythymidine 5'-monophosphate-terminated primer.
 PMID: 12902345       2003       The Journal of biological chemistry
Abstract: Resistance to zidovudine (3'-azido-3'-deoxythymidine, AZT) by the human immunodeficiency virus, type 1, requires multiple amino acid substitutions such as D67N/K70R/T215F/K219Q in the viral reverse transcriptase (RT).


  Non-nucleoside inhibitors of HIV-1 reverse transcriptase inhibit phosphorolysis and resensitize the 3'-azido-3'-deoxythymidine (AZT)-resistant polymerase to AZT-5'-triphosphate.
 PMID: 12917424       2003       The Journal of biological chemistry
Abstract: Here we compared wild type and AZT-resistant (D67N/K70R/T215Y/K219Q) RTs for their ability to unblock the AZTMP-terminated primer by phosphorolysis in the presence of physiological concentrations of pyrophosphate or ATP.


  Mutation patterns of the reverse transcriptase genes in HIV-1 infected patients receiving combinations of nucleoside and non nucleoside inhibitors.
 PMID: 14522102       2003       International journal of antimicrobial agents
Abstract: The frequencies of T215S/Y/F, M41L, D67N, L210W K70R, K219Q mutations, detectable in plasma samples, conferring resistance to zidovudine were 61.2, 56.2, 36.2, 31.5, 27.5 and 17.5%, respectively.


  In vitro study of resistance-associated genotypic mutations to nucleoside analogs.
 PMID: 14565328       2003       Nucleosides, nucleotides & nucleic acids
Abstract: Selected AZT resistant variants contained amino acid substitutions in positions D67A and K70R.


  Lack of persistent drug-resistant mutations evaluated within and between treatment interruptions in chronically HIV-1-infected patients.
 PMID: 14571185       2003       AIDS (London, England)
Abstract: In the remaining six patients, the following patterns of mutations associated with viral resistance were found: one mutation (K70R), which was observed in one patient during the 1st TI and persisted during follow-up; two mutations (L90M, M184V), which were observed in four patients during the 1st TI and were intermittently present or lost following extended TI, treatment reinitiation and/or during subsequent TI; and evolution of two mutations (M184V, K219E) observed in two patients.


  Novel enzyme-linked minisequence assay for genotypic analysis of human immunodeficiency virus type 1 drug resistance.
 PMID: 14605126       2003       Journal of clinical microbiology
Abstract: ELMA is a combination of hybridization and a 1-base extension reaction, and we designed the assay to detect five mutations conferring nucleoside analogue resistance (M41L, D67N, K70R, T215Y, and M184V) and six mutations conferring protease inhibitor resistance (D30N, M46I, G48V, V82A, I84V, and L90M).


  New patterns of HIV-1 resistance during HAART.
 PMID: 14616723       2003       Clinical microbiology and infection
Abstract: Nucleoside analog mutations (NAMs) (M41L, D67N, K70R, L210W, T215Y/F and K219Q/E) are associated with reduced susceptibility to most nucleoside analogs and the nucleotide tenofovir.


  A review of HIV-1 resistance to the nucleoside and nucleotide inhibitors.
 PMID: 14754429       2003       Current drug targets. Infectious disorders
Abstract: There are several major genetic mutational patterns of resistance and cross-resistance that evolve with the NRTIs including the thymidine analog mutations M41L, D67N, K70R, L210W, T215Y, and K219Q/E/W, the non-thymidine mutations M184V, L74V, and K65R, and the multidrug resistant Q151M complex, as well as others.


  Use of the sensitive/less-sensitive (detuned) EIA strategy for targeting genetic analysis of HIV-1 to recently infected blood donors.
 PMID: 11741169       2002       AIDS (London, England)
Abstract: Genetic evidence for drug resistance to zidovudine (K70R) and non-nucleoside analog reverse transcriptase inhibitors (V108I) was detected in one strain each, and three other strains showed the presence of accessory protease inhibitor resistance mutations.


  Frequency of mutations conferring resistance to nucleoside reverse transcriptase inhibitors in human immunodeficiency virus type 1-infected patients in Korea.
 PMID: 11923351       2002       Journal of clinical microbiology
Abstract: The frequencies of K70R, T215S/Y/F (i.e., mutation of T at codon 215 to S, Y, or F), D67N/E, K219Q, T69N/S/A, M41L, and L210W mutations conferring resistance to zidovudine were 57.6, 36.4, 36.4, 27.2, 24.2, 21.2, and 12.1%, respectively.



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